Founder cells

The expansion of founder cells that are originally specified to the cortical held directly affects cerebral cortical size. It has been postulated that founder population expands through symmetric divisions before... 

Apart from these major defects in dorsal mesodermal derivatives, tinman mutants also exhibit more subtle defects in other areas of the mesoderm. For example, a specific subset ol ventral and lateral body wall muscles and their founder cells arc not formed (Figure 2G.H) (Azpiazu and F- rasch, 1993). Moreover, tinman mutant embryos lack the DM cells and their preeursors ([ igure 2I.J) (Gorezykaet af, 1994 ... 

Figure 2. The function of tinman in the formation of mesodermal tissues. The (eft column shows wild-type embryos and the right column tinman mutant embryos of the same stage and stained with the same markers. (A, B) Neither cardioblasts nor pericardial cells are formed in tin mutants (embryos stained as in Figure 1 ). (C, D) The midgut musculature (stained for flCal expression from an enhancer trap insertion is completely m ssing in tinman mutants. (E, F Dorsal muscles (stained for [iCa expression from a .cZ reporter insertion Yin and Frasch, 1998) are not properly specified in tinman mutants. (G, H) Earlv stage 12. The muscle founders of the S59 cluster I (as detected with an S59 antibody), which give rise to muscles 5 and 25, are not specified in tinman mutants. By contrast, the founder cells of S59 cluster II are formed normally and will develop into muscles 26, 2(r, and 29, (I, J) Stage 11. huttonlesi niRN.A expression in the DM cell precursors (arrow) is absent in tin mutants and DM cells are not formed. (The bilateral pairs of nuclei are Eve-stained neuronal precursors).. Abbreviations DM dorsal median cell precursors dsm dorsal somatic muscles mgv m midgut visceral mesoderm pc pericardial precursors.

B. The Founder Cell Concept of Somatic Muscle Development... 

C. Genetic Mechanisms in Formation and Specification of Founder Cells Segregation and Specification of Muscle Founders... 

How does numb determine the identities of these founder cells Apparently, it does so, at least in part, by regulating the maintenance of Kr and S59 expression in the founder cell of muscle 27 that inherits Numb protein. By contrast, its sibling lacks Numb protein, which results in the downregulation of Kr and S59, and consequently this cell assumes the identity as a founder cell of muscle 26. Kr seems to act upstream of S59 in this maintenance process. Thus, in ifr mutants, S59 is not maintained in either of the two founder cells and both develop into muscle 26, while upon ectopic Kr expression in all myoblasts, both maintain S59 expression and develop into muscle 27 (Ruiz Gomez and Bate, 1997). 

Kr in the m 26 founder, whereas the presence of Numb in the m 27 founder blocks this activity, thereby allowing A r expression to be maintained (Figure 4). A major question for the future will be how the asymmetry in the muscle progenitor is established initially, an attribute that ultimately determines the differential development of the sibling founder cells and the muscles derived from them. 

Baylies, M., Martinez Arias, A., and Bate, M. (1995). wingless is required for the formation of a subset of muscle founder cells during Drosophila embryogenesis. Development 121 3 19-31 X1. 

As the cells grow in this aerobic cultivation at a rate of 0.39 X 10 cell/(mL-day), oxygen from air is consumed at the rate of 0.2 X 10 mol 02/(cell-hr), and tPA is produced at the rate of 50 pico gram tPA/(cell-day). The latter is secreted gradually into the liquid media solution. Note that reaction (3.8) is carried out once during the research and development phase. Initially, 1-10 mg of tPA-DNA are added to 10 cells to produce a few tPA-CHO cells in many unmodified CHO cells. After careful selection, one tPA-CHO cell (the founder cell) is selected and amplified to yield about 10 cells/mL in 10-1(X) L. These cells are frozen in aliquots. 

---